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The METTL3-YTHDC1 axis mediates architectural RNA m6A modification to modulate the integrity of chromatin TADs in MLLr+ AML genome

GSE287825 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 36 samples Submitted 2026/02/11 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 36 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Homo sapiens (human)
Topic
Acute myeloid leukemiaThis series is part of our curated briefing on it.
Samples
36 samples: 32 distinct titles, 4 of them repeatedGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
The METTL3-YTHDC1 axis mediates architectural RNA m(6)A modification to modulate the integrity of chromatin TADs in MLLr + AML genomeMolecular cancer · 2025
Summary (written by the submitters)
Methyltransferase-like protein 3 (METTL3) as a key regulator of leukemia-associated gene expression in acute myeloid leukemia (AML) contributes to malignant transformation. Chromatin topologically associating domains (TADs) are essential for maintaining the structural integrity and activity of the AML genome. However, the regulatory mechanism by which METTL3 facilitates the integrity and activity of chromatin TADs leading to AML progression remains unknown.
Read the full summary ↓
Our findings demonstrate that METTL3 has a specific interaction with YTHDC1, METTL3 and CCCTC-binding factor (CTCF) by METTL3 immunoprecipitation-mass spectrometry (IP-MS) analysis in MLLr+ AML cells. METTL3 colocalizes with CTCF at the promoters and enhancers of the MLLr+ AML genome by analysis of METTL3 ChIP-seq and CTCF ChIP-seq. Notably, METTL3 is highly upregulated in MLLr+ AML cells. Depletion of METTL3 significantly impacts CTCT binding sites (CBSs) and chromatin accessibility at the promoters and enhancers of key leukemia genes, such as MYB and RUNX1, resulting in reduced leukemia gene expression and impaired cell proliferation. Critically, high-resolution chromatin conformation capture (Hi-C) data indicates that YTHDC1 loss substantially disrupts CTCF-dependent 3D genome organization. Furthermore, disruption of chromatin architectural RNAs (arcRNAs) mediated R-loops influences the chromatin TAD structures at specific leukemia signature gene loci. YTHDC1 recognizes m6A-modified arcRNAs, enhancing their formation of R-loops to maintain the CTCF-dependent TADs in MLLr+ AML genome. This interaction is crucial for regulating oncogenic TAD boundary activity and integrity to modulate the transcription of leukemia signature genes. In conclusion, the METTL3-YTHDC1-CTCF axis plays a critical role in regulating the expression of AML signature genes through facilitating AML genome organization. These findings provide a valuable theoretical insight for identifying new therapeutic targets in AML treatment.
Published in
The METTL3-YTHDC1 axis mediates architectural RNA m(6)A modification to modulate the integrity of chromatin TADs in MLLr + AML genome
Fu R, Yu W, Zhao R et al. · Molecular cancer 2025 · PMID 41430607 · doi:10.1186/s12943-025-02545-x
This dataset
Open GSE287825 in finder → Find more human RNA-seq datasets → Acute myeloid leukemia landscape →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE287825_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1214812 and SRA study SRP559475. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41430607) ↗
Study design
32 distinct titles, 4 of them repeated
MOLM13, Control, Ctrl ×2 MOLM13, shYTHDC1, shYTH ×2 MOLM13, shMETTL3, shMET ×2 MOLM13, APEX, sgRX ×2

How we read this: Read from 36 sample titles: 32 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
More Acute myeloid leukemia datasets

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